The objective of this project is to determine in the primate whether a short acting barbiturate given for 12 hours beginning within 30 minutes after embolic occlusion of the middle cerebal artery reduces the clinical and/or pathological sequelae observed in the first five days after the infarct. And to establish the pathophysiologic basis for the observed protective effect by continuous monitoring of superficial and deep cerebral blood flow and EEG. Cerebral infarction might be delayed by reducing metabolic demand while secondary supply sources improve or are restored. Hydrogen polarographic blood flow methods permit separation of blood flow values into cortical and basal ganglia components. Compared to a control group, animals treated with barbiturate regained grasp, movement, and some strength in affected limbs. Untreated animals did not improve measurably in these areas during the five-day observation period. Pathologically, the untreated monkeys have both cortical and deep infarction, while treated animals have relative cortical spring. Furthermore, the morphological changes due to ischemia develop at a slower rate in treated animals. Physiologically, CBF changes occur over the same time axis after embolism in barbiturate and ketamine treated groups. EEG changes, however, are more prominent in ketamine animals due to the higher amplitudes and baseline frequencies in pre-embolic control.